2013
DOI: 10.3390/ijms140815931
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Mechanisms of Radiation Toxicity in Transformed and Non-Transformed Cells

Abstract: Radiation damage to biological systems is determined by the type of radiation, the total dosage of exposure, the dose rate, and the region of the body exposed. Three modes of cell death—necrosis, apoptosis, and autophagy—as well as accelerated senescence have been demonstrated to occur in vitro and in vivo in response to radiation in cancer cells as well as in normal cells. The basis for cellular selection for each mode depends on various factors including the specific cell type involved, the dose of radiation… Show more

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Cited by 93 publications
(74 citation statements)
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References 195 publications
(284 reference statements)
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“…Senescence is linked to various phenotypes including b-galactosidase expression, telomere maintenance defect and metabolic modifications. However, radiation-induced cell senescence is certainly more complex than a simple mitosis arrest related to telomere shortening, especially in mainly quiescent primary cells such as articular chondrocytes (84). The molecular mechanisms of radiation-induced cell senescence are driven by the triumvirate ATM-p53-p21 (85) and may be modulated by wild-type p53-inducible phosphatase-1 protein (Wip1) (86).…”
Section: Senescence Of Irradiated Chondrocytesmentioning
confidence: 99%
“…Senescence is linked to various phenotypes including b-galactosidase expression, telomere maintenance defect and metabolic modifications. However, radiation-induced cell senescence is certainly more complex than a simple mitosis arrest related to telomere shortening, especially in mainly quiescent primary cells such as articular chondrocytes (84). The molecular mechanisms of radiation-induced cell senescence are driven by the triumvirate ATM-p53-p21 (85) and may be modulated by wild-type p53-inducible phosphatase-1 protein (Wip1) (86).…”
Section: Senescence Of Irradiated Chondrocytesmentioning
confidence: 99%
“…Necrosis results typically from a high magnitude of stress after either apoptosis or cellular senescence. Depending on the cell lines, it can be triggered by low or very high doses of IR (27). Moreover, human mesenchymal cells (precursors of chondrocytes), in contrast to arthritic chondrocytes, do not undergo radiation-induced apoptosis, probably owing to the efficient activation of the DNA damage response pathways (6,33).…”
Section: Discussionmentioning
confidence: 99%
“…Depending on the radiation quality, irradiation dose, or cell type, IR can induce several types of cell death (27). Necrosis and apoptosis were analyzed in 2D HACs, with no significant induction until 96 hours after irradiation ( Fig.…”
Section: Differential Senescence Induction In 2d Hacs and 3dcam Aftermentioning
confidence: 99%
“…Effects on normal tissue often limiting clinical use of radiation involves delayed cycles of inflammation, tissue dysfunction, atrophy, and/or fibrotic remodeling (Panganiban et al 2013). Studies point out that low apoptotic response is associated with risk for development of late side effects, which occur around 6 months to many years after exposure and, thus, demanding follow-up relatively long.…”
Section: Discussionmentioning
confidence: 99%